HIPK1 Interference Attenuates Inflammation and Oxidative Stress of Acute Lung Injury via Autophagy

BACKGROUND: Acute respiratory distress syndrome (ARDS), which is characterized by severe hypoxemia (PaO(2)/FIO(2) ≤300 mmHg), is usually companied by uncontrolled inflammation, oxidative injury, and the damage to the alveolar-capillary barrier. Severe ARDS is usually companied with acute lung injury that worsen the patients’ condition. HIPK1 is a modulator of homeodomain-containing transcription factors and regulates multiple cellular biological process associated with inflammation and anti-stress responses. MATERIAL/METHODS: We used an LPS-induced mouse acute lung injury (ALI) model to investigate the possible role of HIPK1 in ALI pathophysiology. RESULTS: We found the HIPK1 was elevated in ALI model mice while interference of HIPK1 by siRNA attenuated the inflammation and oxidative stress indicators (H(2)O(2), O(−)(2), and NO). Further research found HIPK1 interference enhanced the autophagy. CONCLUSIONS: Decreased HIPK1 in ALI showed protective effects in attenuating inflammation and oxidative stress and enhancing autophagy, indicating HIPK1 as a possible target in ALI management.